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Human periodontal ligament cells (hPDLCs) are important source of periodontal tissue reconstruction. Under chronic inflammation, the multi-directional differentiation potential and chemotaxis in hPDLCs are decreased. Therefore, inhibiting inflammatory microenvironment and improving the functional characteristics of stem cells can better promote periodontal tissue reconstruction. This study was to investigate the effect of astaxanthin (AST) on lipopolysaccharide (LPS)-induced inflammation in hPDLCs and the underlying mechanisms.

hPDLCs were isolated and cultured in vitro, and vimentin and keratin immunocytochemical staining were used to identify hPDLCs. CCK-8 assay was used to measure the effects of AST (1, 5, 10, 20, 50, 100, and 200 μmol/L) on proliferation of hPDLCs. Quantitative RT-PCR (RT-qPCR) and ELISA were used to measure the mRNA and protein expression of inflammatory factors (IL-6, IL-1β, and TNF-α) in the control (Con) group, the LPS group, and the LPS+AST (5, 10, 20, and 50 μmol/L) group. Selleckchem Pargyline Westesm and p65 in nucleus of the LPS group were significantly up-regulated (both

<0.05). Compared with the LPS group, the levels of IKBα and p65 in cytoplasm of the LPS+AST (20 μmol/L) group were significantly upregulated (both

<0.05), and the levels of p-IKBα in cytoplasm and p65 in nucleus of the LPS+AST (20 μmol/L) group were significantly downregulated (both

<0.05). The mRNA and protein expressions of IL-6, IL-1β, and TNF-α in the LPS+PDTC (10 μmol/L) group were lower than those in the LPS group (all

<0.05).

AST promotes the proliferation of hPDLCs, which is related to suppression of LPS-induced the secretion of inflammatory factors via inhibiting the activation of NF-κB signaling pathway.

AST promotes the proliferation of hPDLCs, which is related to suppression of LPS-induced the secretion of inflammatory factors via inhibiting the activation of NF-κB signaling pathway.

To investigate the role of autophagy in oxalate-induced toxicity of human proximal renal tubular epithelial cell (HK-2).

HK-2 cells were exposed to oxalate (1 mmol/L) for 2 h and 3-methyladenine (3-MA) was used to inhibit autophagy. Then Western blotting was used to measure the expression of autophagy-related protein LC3II. Cell viability and cell apoptosis were measured by MTT assay and flow cytometry assay, respectively.

Cytoplasmic vacuolization was observed in HK-2 cells after treating with oxalate for 2 h. However, 3-MA showed no effects on the formation of cytoplasmic vacuolization regardless of the dose at 1 or 5 mmol/L. The expression of LC3II protein was significantly increased in the HK-2 cells in the presence of oxalate (0.62±0.03 vs 0.35±0.02,

<0.05). The expression of LC3II protein in HK-2 cells was downregulated by 3-MA at both 1 and 5 mmol/L compared with the blank control (0.17±0.03 vs 0.35±0.02, 0.16±0.03 vs 0.35±0.02, both

<0.05). Oxalate-induced upregulation of LC3II was reversed by 3-MA only at the concentration of 5 mmol/L (0.47±0.04 vs 0.62±0.03,

<0.05) rather than 1 mmol/L (0.61±0.04 vs 0.62±0.03,

>0.05). Oxalate attenuated viability [(77.32±2.69)% vs 100%,

<0.05] and increased the apoptosis [(8.32±1.05)% vs (2.36±0.29)%,

<0.05] in HK-2 cells, and these effects were reversed by 3-MA only at the concentration of 5 mmol/L [(91.91±3.36)% vs (77.32±2.69)%, (3.45±0.21)% vs (8.32±1.05)%, respectively, both

<0.05] rather than 1 mmol/L [(80.48±3.41)% vs (77.32±2.69)%, (7.81±0.47)% vs (8.32±1.05)%, both

>0.05, respectively].

Autophagy of HK-2 cells is enhanced by oxalate at the concentration of 1 mmol/L. Inhibition of 3-MA-induced autophagy protects HK-2 cells from the oxalate-induced cytotoxicity.

Autophagy of HK-2 cells is enhanced by oxalate at the concentration of 1 mmol/L. Inhibition of 3-MA-induced autophagy protects HK-2 cells from the oxalate-induced cytotoxicity.

Although numerous studies have investigated obesity's negative effect on coronavirus disease 2019 (COVID-19) outcomes, only a limited number focused on this association in diabetic patients. In this study, we analyzed the association between obesity and COVID-19 outcome (death, intensive care unit [ICU] admission, mechanical ventilation needs, quick Sequential Organ Failure Assessment [qSOFA] score, and confusion, urea, respiratory rate, blood pressure [CURB-65] scores) for hospitalized diabetic patients.

In this prospective hospital-based registry of patients with COVID-19 in East Azerbaijan, Iran, 368 consecutive diabetic patients with COVID-19 were followed from admission until discharge or death. Self-reported weight and height were used to calculate body mass index (kg/m

) upon admission. Our primary endpoint was analyzing obesity and COVID-19 mortality association. Assessing the associations among obesity and disease severity, ICU admission, and mechanical ventilation was our secondary endpoint.

We analyzed data from 317 patients and found no significant difference between obese and non-obese patients regarding frequency of death, invasive mechanical ventilation, ICU admission, CURB-65, or qSOFA scores (

>0.05). After adjusting for confounding factors, obese diabetic COVID-19 patients were 2.72 times more likely to die than non-obese patients. Moreover, ventilator dependence (adjusted odds ratio [aOR], 1.87; 95% confidence interval [CI], 1.03-4.76) and ICU admission (aOR, 2.41; 95% CI, 1.11-5.68) odds were significantly higher for obese patients than non-obese patients.

The results of the present study indicated that obesity worsens health outcomes for diabetic COVID-19 patients.

The results of the present study indicated that obesity worsens health outcomes for diabetic COVID-19 patients.

We aimed to explore empathy, moral competencies, callous traits, and temperament in a sample of medical students. Furthermore, we aimed to investigate differences in our variables across the 1st and 5th years of medical education and possible correlations between them.

This was a cross-sectional study with 138 medical students. We resorted to self-reported instruments that were given at the end of classes Barrett-Lennard Relational Inventory, Temperament Evaluation of Memphis, Pisa and San Diego Auto-questionnaire, Inventory of Callous-Unemotional Traits, and Moral Competence Test. For the statistical analysis, we resorted to descriptive and inferential statistics, using non-parametric tests when data didn't follow a normal distribution.

We found no statistical difference between empathy scores in 1st (N=104, Mean=41.42, SD=22.48) and 5th year students (N=34, Mean=37.35, SD=23.35), t

=0.908, p=0.366. Callous traits were negatively correlated with empathy (r

=-0.444, p=0.000) and no correlation between moral competences and empathy (r

=0.

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